Search results for "Microarray"

showing 10 items of 401 documents

Poor transcript-protein correlation in the brain: negatively correlating gene products reveal neuronal polarity as a potential cause

2018

Transcription, translation, and turnover of transcripts and proteins are essential for cellular function. The contribution of those factors to protein levels is under debate, as transcript levels and cognate protein levels do not necessarily correlate due to regulation of translation and protein turnover. Here we propose neuronal polarity as a third factor that is particularly evident in the CNS, leading to considerable distances between somata and axon terminals. Consequently, transcript levels may negatively correlate with cognate protein levels in CNS regions, i.e., transcript and protein levels behave reciprocally. To test this hypothesis, we performed an integrative inter-omics study a…

Male0301 basic medicineneuronal polarityintegrative omics[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyBiologynegative transcript|protein correlationProteomicsBiochemistryRats Sprague-DawleyTranscriptome03 medical and health sciencesCellular and Molecular Neurosciencetranscriptomics0302 clinical medicineproteomicsTranscription (biology)[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsRNA MessengerGeneNeuronsProtein turnoverBrainCell PolarityProteinsRatsTransport proteinCell biology030104 developmental biologySuperior olivary complexprotein transportFemaleDNA microarray030217 neurology & neurosurgery
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation.

2014

The Ewing sarcoma family of tumors (EFT) is a group of highly malignant small round blue cell tumors occurring in children and young adults. We report here the largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines). Using a combination of whole genome sequencing and targeted sequencing approaches, we discover that EFT has a very low mutational burden (0.15 mutations/Mb) but frequent deleterious mutations in the cohesin complex subunit STAG2 (21.5% tumors, 44.4% cell lines), homozygous deletion of CDKN2A (13.8% and 50%) and mutations of TP53 (6.2% and 71.9%). We additionally note an increased prevalence of the BRCA2 K3326X polymorphism in EFT patient samples (7.3%) compared …

MaleCancer ResearchCell Cycle Proteinsmedicine.disease_causeFusion geneCDKN2AMedicine and Health Sciences2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)CancerPediatricMutationTissue microarrayTumorGenomeSarcomasHigh-Throughput Nucleotide SequencingAntigens NuclearSarcomaNeoplasm ProteinsOncologyChild PreschoolFemaleSarcomaResearch ArticleBiotechnologyHumanAdultPediatric Research Initiativelcsh:QH426-470Cohesin complexAdolescentPediatric CancerEwing SarcomaSarcoma EwingBiologyDisease-Free SurvivalFrameshift mutationCell LineGermline mutationRare DiseasesCell Line TumorEwingCancer GeneticsmedicineGeneticsHumansNuclearGenetic TestingAntigensPreschoolMolecular BiologyEcology Evolution Behavior and SystematicsGenome HumanHuman GenomeBiology and Life SciencesCancers and NeoplasmsInfantmedicine.diseaselcsh:GeneticsOrphan DrugMutationCancer researchGene DeletionDevelopmental Biology
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Growth Arrest Specific 1 (Gas1) Gene Overexpression in Liver Reduces the In Vivo Progression of Murine Hepatocellular Carcinoma and Partially Restore…

2015

The prognosis of hepatocellular carcinoma patients is usually poor, the size of tumors being a limiting factor for surgical treatments. Present results suggest that the overexpression of Gas1 (growth arrest specific 1) gene reduces the size, proliferating activity and malignancy of liver tumors. Mice developing diethylnitrosamine-induced hepatocellular carcinoma were subjected to hydrodynamic gene delivery to overexpress Gas1 in liver. This treatment significantly (p < 0.05) reduced the number of large tumors, while the difference in the total number of lesions was not significant. Moreover, the number of carcinoma foci in the liver and the number of lung metastases were reduced. These resu…

MaleCarcinoma Hepatocellularlcsh:MedicineCell Cycle ProteinsGene deliveryBiologyGPI-Linked ProteinsReal-Time Polymerase Chain ReactionTransfectionMiceCell Line TumorGene expressionCarcinomamedicineAnimalslcsh:ScienceLungCell ProliferationRegulation of gene expressionMultidisciplinaryMicroarray analysis techniquesLiver Neoplasmslcsh:RCell cyclemedicine.diseaseMolecular biologyHedgehog signaling pathwayGene Expression Regulation NeoplasticLiverHepatocellular carcinomaDisease ProgressionHydrodynamicslcsh:QResearch ArticlePLoS ONE
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Improving cytocompatibility of Co28Cr6Mo by TiO 2 coating: gene expression study in human endothelial cells

2013

Cobalt-based materials are widely used for coronary stents, as well as bone and joint implants. However, their use is associated with high corrosion incidence. Titanium alloys, by contrast, are more biocompatible owing to the formation of a relatively inactive titanium oxide (TiO 2 ) layer on their surface. This study was aimed at improving Co28Cr6Mo alloy cytocompatibility via sol–gel TiO 2 coating to reduce metal corrosion and metal ion release. Owing to their role in inflammation and tissue remodelling around an implant, endothelial cells present a suitable in vitro model for testing the biological response to metallic materials. Primary human endothelial cells seeded on Co28Cr6Mo showe…

MaleCell typeBiocompatibilityBiomedical EngineeringBiophysicsBioengineeringInflammationBiochemistryBiomaterialsCoated Materials BiocompatibleMaterials TestingGene expressionmedicineHumansResearch ArticlesCells CulturedOligonucleotide Array Sequence AnalysisTitaniumRegulation of gene expressionChemistryMicroarray analysis techniquesGene Expression ProfilingMetallurgytechnology industry and agricultureEndothelial CellsProstheses and ImplantsCell biologyEndothelial stem cellGene expression profilingGene Expression RegulationFemaleChromium Alloysmedicine.symptomBiotechnologyJournal of The Royal Society Interface
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Molecular Pathways Involved in Prostate Carcinogenesis: Insights from Public Microarray Datasets

2012

PLoS one 7(11), e49831 (2012). doi:10.1371/journal.pone.0049831

MaleEXPRESSIONMicroarrayMicroarraysPopulationlcsh:MedicineBiologyMETABOLISMMalignancyBioinformaticsMetastasisMolecular GeneticsProstate cancerGeneticsCancer GeneticsBiomarkers TumormedicineHumansEpithelial–mesenchymal transitioneducationProstate carcinogenesislcsh:ScienceBiologyCANCER CELLSSIGNATURESOligonucleotide Array Sequence Analysiseducation.field_of_studyMultidisciplinarySystems BiologyProstate CancerCHOLESTEROLlcsh:RComputational BiologyCancers and NeoplasmsProstatic NeoplasmsGenomicsmedicine.diseaseEPITHELIAL-MESENCHYMAL TRANSITIONGene Expression Regulation NeoplasticMODELGenitourinary Tract TumorsCell Transformation NeoplasticOncologyCancer cellBIOLOGICAL PATHWAYSMedicinelcsh:QMetabolic Networks and PathwaysResearch Article
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Transcriptional profiling of rat hypothalamus response to 2,3,7,8-tetrachlorodibenzo-ρ-dioxin

2015

In some mammals, halogenated aromatic hydrocarbon (HAH) exposure causes wasting syndrome, defined as significant weight loss associated with lethal outcomes. The most potent HAH in causing wasting is 2,3,7,8-tetrachlorodibenzo-r-dioxin (TCDD), which exerts its toxic effects through the aryl hydrocarbon receptor (AHR). Since TCDD toxicity is thought to predominantly arise from dysregulation of AHR-transcribed genes, it was hypothesized that wasting syndrome is a result of to TCDD-induced dysregulation of genes involved in regulation of food-intake. As the hypothalamus is the central nervous systems' regulatory center for food-intake and energy balance. Therefore, mRNA abundances in hypothala…

MaleFOOD-INTAKETCDDPolychlorinated DibenzodioxinsTime FactorsTranscription GeneticMicroarrayTISSUE GROWTH-FACTORAHRAH GENE BATTERY413 Veterinary scienceToxicologyToxicogeneticsfeed restrictionTranscriptomeNAD(P)H Dehydrogenase (Quinone)RESISTANT RATheterocyclic compoundsMESSENGER-RNA EXPRESSIONhypothalamusWastingreproductive and urinary physiologyOligonucleotide Array Sequence Analysisbiologyta31413. Good healthPROBE LEVELHypothalamusToxicityENERGY-BALANCEmedicine.symptommicroarrayARYL-HYDROCARBON RECEPTORendocrine systemmedicine.medical_specialtyta3111Species SpecificityInternal medicineCytochrome P-450 CYP1A1medicineAnimalsRats Long-EvansRNA MessengerWasting SyndromeRats WistarWasting SyndromeGene Expression Profilingta1184Lethal doseAryl hydrocarbon receptorstomatognathic diseasesEndocrinologyINDUCED ANOREXIAGene Expression Regulationbiology.proteinToxicology
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Bayesian model to detect phenotype-specific genes for copy number data

2012

Abstract Background An important question in genetic studies is to determine those genetic variants, in particular CNVs, that are specific to different groups of individuals. This could help in elucidating differences in disease predisposition and response to pharmaceutical treatments. We propose a Bayesian model designed to analyze thousands of copy number variants (CNVs) where only few of them are expected to be associated with a specific phenotype. Results The model is illustrated by analyzing three major human groups belonging to HapMap data. We also show how the model can be used to determine specific CNVs related to response to treatment in patients diagnosed with ovarian cancer. The …

MaleGenotypeGene DosageHapMap ProjectBiologylcsh:Computer applications to medicine. Medical informaticsPopulation stratificationBayesian inferencePolymorphism Single NucleotideBiochemistry03 medical and health sciencesBayes' theorem0302 clinical medicineStructural BiologymedicineHumansComputer SimulationGenetic Predisposition to DiseaseGenetic TestingCopy-number variationInternational HapMap Projectlcsh:QH301-705.5Molecular Biology030304 developmental biologyGenetic testingGenetics0303 health sciencesModels StatisticalModels Geneticmedicine.diagnostic_testMethodology ArticleApplied MathematicsConfoundingBayes Theorem3. Good healthComputer Science ApplicationsPhenotypelcsh:Biology (General)030220 oncology & carcinogenesislcsh:R858-859.7FemaleDNA microarrayAlgorithmsBMC Bioinformatics
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Genomic response of the rat brain to global ischemia and reperfusion

2008

To identify genes that are involved in ischemia response of the brain, we have evaluated changes of gene expression in rat cerebrum after 15 min complete global ischemia, followed by reperfusion for 1 h, 6 h or 24 h. The expression profiles of approximately 30,000 transcripts from three subjects in each group (including sham-operated controls) were monitored employing oligonucleotide microarrays. About 20,000 transcripts were detectable in rat brains. The levels of 576 transcripts (approximately 2.9%) were significantly altered in response to experimental ischemia. 419 transcripts were up- and 157 downregulated; 39 transcripts changed after 1 h reperfusion, 174 after 6 h and 462 after 24 h.…

MaleMicroarrayIschemiaBiologyBrain IschemiaGene expressionmedicineAnimalsCluster AnalysisRats WistarMolecular BiologyOligonucleotide Array Sequence AnalysisRegulation of gene expressionReverse Transcriptase Polymerase Chain ReactionMicroarray analysis techniquesGene Expression ProfilingGeneral NeuroscienceBrainmedicine.diseaseMolecular biologyRatsGene expression profilingReverse transcription polymerase chain reactionReal-time polymerase chain reactionGene Expression RegulationReperfusionRNANeurology (clinical)Developmental BiologyBrain Research
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The Choice of the Filtering Method in Microarrays Affects the Inference Regarding Dosage Compensation of the Active X-Chromosome

2011

BackgroundThe hypothesis of dosage compensation of genes of the X chromosome, supported by previous microarray studies, was recently challenged by RNA-sequencing data. It was suggested that microarray studies were biased toward an over-estimation of X-linked expression levels as a consequence of the filtering of genes below the detection threshold of microarrays.Methodology/principal findingsTo investigate this hypothesis, we used microarray expression data from circulating monocytes in 1,467 individuals. In total, 25,349 and 1,156 probes were unambiguously assigned to autosomes and the X chromosome, respectively. Globally, there was a clear shift of X-linked expressions toward lower levels…

MaleMicroarrayMicroarraysScienceGene ExpressionBiologyMonocytesGenomic ImprintingMiceX Chromosome InactivationGenes X-LinkedDosage Compensation GeneticMolecular Cell BiologyGeneticsAnimalsHumansRNA MessengerBiologyX-linked recessive inheritanceX chromosomeOligonucleotide Array Sequence AnalysisGeneticsChromosomes Human XMultidisciplinaryDosage compensationAutosomeModels GeneticChromosome BiologyGene Expression ProfilingQRComputational BiologyGenomicsGene expression profilingHEK293 CellsMedicineEpigeneticsFemaleDNA microarrayGenomic imprintingGenome Expression AnalysisResearch ArticlePLoS ONE
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SNPs array karyotyping reveals a novel recurrent 20p13 amplification in primary myelofibrosis.

2011

The molecular pathogenesis of primary mielofibrosis (PMF) is still largely unknown. Recently, single-nucleotide polymorphism arrays (SNP-A) allowed for genome-wide profiling of copy-number alterations and acquired uniparental disomy (aUPD) at high-resolution. In this study we analyzed 20 PMF patients using the Genome-Wide Human SNP Array 6.0 in order to identify novel recurrent genomic abnormalities. We observed a complex karyotype in all cases, detecting all the previously reported lesions (del(5q), del(20q), del(13q), +8, aUPD at 9p24 and abnormalities on chromosome 1). In addition, we identified several novel cryptic lesions. In particular, we found a recurrent alteration involving cytob…

MaleMicroarraysMIELOFIBROSISChromosomes Human Pair 20Loss of Heterozygositylcsh:MedicineLoss of heterozygosityCohort StudiesHematologic Cancers and Related DisordersGene duplicationTaq Polymeraselcsh:ScienceOligonucleotide Array Sequence AnalysisMultidisciplinaryMYELOFIBROSIS; SNPKaryotypeGenomicsHematologyUniparental disomyMedicineFemaleImmunohistochemical AnalysisSNP arrayResearch ArticleTest Evaluationmedicine.medical_specialtyDNA Copy Number VariationsImmunologySNPLocus (genetics)Single-nucleotide polymorphismReceptors Cell SurfaceBiologyPolymorphism Single NucleotideDiagnostic MedicinemedicineGeneticsHumansBiologyAgedEvolutionary BiologyMyeloproliferative DisordersPopulation Biologylcsh:RCytogeneticsGene AmplificationComputational BiologyDNAUniparental Disomymedicine.diseaseMolecular biologyMYELOFIBROSISPrimary MyelofibrosisKaryotypingGenetic PolymorphismImmunologic TechniquesClinical Immunologylcsh:QPopulation GeneticsPLoS ONE
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